[jackD]

I love my Brain Sprouts I feed them daily some Brain Tonic that is full of "neurotrophic growth factors".

"Numerous neurotrophic growth factors help determine which neurons develop in the immature brain and which are retained in the adult brain. Neurotrophic factors can also induce neurons to sprout axons capable of growing into new locations and forming new synaptic connections, a process that continues in the mature brain."


http://www.psychiatrist.com/pcc/brainstorm/br5904.htm (main article)

http://www.psychiatrist.com/pcc/brainstorm/br5906.htm (therapeutic potential)

http://www.psychiatrist.com/pcc/brainstorm/br5806.htm (Glutamate assassin/excitotoxic neuron murder)

The Second Stage of MS is "The Degererative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage".

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

http://home.ix.netcom.com/~jdalton/two%20stage%20MS.jpg

Braindead

p.s Other good info here also:

http://www.psychiatrist.com/pcc/brainstorm/

[SallyC]

Hey Jack, long time no see. Welcome back.
I've missed your posts.

Do you really believe in this brain food? Any
bad sides? Is it working for you? Which Brain
Tonic is the best?

How have you been.

[jackD]

One of the KEY "neurotrophic growth factors" is a substance called NERVE GROWTH FACTOR - NGF.

This is probably the single most practical ingredient in any contemporary "Brain Tonic" that one could take.

The problem with NGF when taken orally is that it does not make it through the BBB Blood Brain Barrier. Drilling a hole in the Brain and literally pouring some in does work, but has some practical limitations.

However NGF is GREAT for those small Brain repair jobs. (pun intended)

But it is not hopeless because some "things" that make it through the BBB can cause the Brain to make more NGF itself.

One of these substances is well known to MS folks - Vitamin D3. So it is a good idea to take plenty -year round!

Braindead

1: Neurosci Lett. 2003 Jun 5;343(2):139-43.

1,25-dihydroxy (vitamin D3) induces nerve growth factor, promotes neurite outgrowth and inhibits mitosis in embryonic rat hippocampal neurons.Brown J, Bianco JI, McGrath JJ, Eyles DW.
School of Biomedical Sciences, University of Queensland, Brisbane, Qld 4072, Australia.

There is an accumulation of evidence implicating a role for vitamin D(3) in the developing brain. The receptor for this seco-steroid is expressed in both neurons and glial cells, it induces nerve growth factor (NGF) and it is a potent inhibitor of mitosis and promoter of differentiation in numerous cells.

We have therefore assessed the direct effect of vitamin D(3) on mitosis, neurite outgrowth, as well as NGF production as a possible mediator of those effects, in developing neurons. Using cultured embryonic hippocampal cells and explants we found the addition of vitamin D(3) significantly decreases the percentage of cultured hippocampal cells undergoing mitosis in conjunction with increases in both neurite outgrowth and NGF production.

The role of vitamin D(3) during brain development warrants closer scrutiny.

PMID: 12759183 [PubMed - indexed for MEDLINE]

1: Behav Brain Res. 1997 Feb;83(1-2):117-22.Links
Orally active NGF synthesis stimulators: potential therapeutic agents in Alzheimer's disease.Yamada K, Nitta A, Hasegawa T, Fuji K, Hiramatsu M, Kameyama T, Furukawa Y, Hayashi K, Nabeshima T.
Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Japan.

The degeneration of cholinergic neurons may be responsible for cognitive impairment in patients with Alzheimer's disease (AD). Since nerve growth factor (NGF) plays an important role in the survival and maintenance of cholinergic neurons in the central nervous system, this factor may have some beneficial effects on the cognitive impairment observed in patients with AD. However, since NGF does not cross the blood-brain barrier and is easily metabolized when administered peripherally, it can only be used when directly injected into the brain. In this review, we show that repeated oral administration of the NGF synthesis stimulators, idebenone and propentofylline, partially restored the age-associated decrease of NGF in the frontal and parietal cortices. Furthermore, this treatment attenuated the impairment of performance in the water maze, passive avoidance, and habituation tasks in rats with bilateral forebrain lesions, and in rats which had received continuous infusion of anti-NGF antibody into the septum. The behavioral improvement induced by idebenone and propentofylline was accompanied by recovery of both the reduced activity of choline acetyltransferase and the changes in [3H]QNB binding. These results suggest that the use of NGF synthesis stimulators may provide a novel therapeutic approach to cholinergic dysfunction.

PMID: 9062669 [PubMed - indexed for MEDLINE]



1: Expert Opin Investig Drugs. 2000 Apr;9(4):747-64. Links
Apoptosis modulators in the therapy of neurodegenerative diseases.Deigner HP, Haberkorn U, Kinscherf R.
Anatomy and Cell Biology III University of Heidelberg, Germany.

Apoptosis is a prerequisite to model the developing nervous system. However, an increased rate of cell death in the adult nervous system underlies neurodegenerative disease and is a hallmark of multiple sclerosis (MS) Alzheimer's- (AD), Parkinson- (PD), or Huntington's disease (HD). Cell surface receptors (e.g., CD95/APO-1/Fas; TNF receptor) and their ligands (CD95-L; TNF) as well as evolutionarily conserved mechanisms involving proteases, mitochondrial factors (e.g. , Bcl-2-related proteins, reactive oxygen species, mitochondrial membrane potential, opening of the permeability transition pore) or p53 participate in the modulation and execution of cell death. Effectors comprise oxidative stress, inflammatory processes, calcium toxicity and survival factor deficiency. Therapeutic agents are being developed to interfere with these events, thus conferring the potential to be neuroprotective. In this context, drugs with anti-oxidative properties, e.g., flupirtine, N-acetylcysteine, idebenone, melatonin, but also novel dopamine agonists (ropinirole and pramipexole) have been shown to protect neuronal cells from apoptosis and thus have been suggested for treating neurodegenerative disorders like AD or PD. Other agents like non-steroidal anti-inflammatory drugs (NSAIDs) partly inhibit cyclooxygenase (COX) expression, as well as having a positive influence on the clinical expression of AD. Distinct cytokines, growth factors and related drug candidates, e.g., nerve growth factor (NGF), or members of the transforming growth factor-beta (TGF-beta ) superfamily, like growth and differentiation factor 5 (GDF-5), are shown to protect tyrosine hydroxylase or dopaminergic neurones from apoptosis. Furthermore, peptidergic cerebrolysin has been found to support the survival of neurones in vitro and in vivo. Treatment with protease inhibitors are suggested as potential targets to prevent DNA fragmentation in dopaminergic neurones of PD patients. Finally, CRIB (cellular replacement by immunoisolatory biocapsule) is an auspicious gene therapeutical approach for human NGF secretion, which has been shown to protect cholinergic neurones from cell death when implanted in the brain. This review summarises and evaluates novel aspects of anti-apoptotic concepts and pharmacological intervention including gene therapeutical approaches currently being proposed or utilised to treat neurodegenerative diseases.

PMID: 11060707 [PubMed - indexed for MEDLINE]
__________________

[jackD]

Folks you had better hurry-- the SALE on my "Brain Tonic" will be over in a few days!!!

Braindead

[jackD]

1: Prog Brain Res. 2004;146:403-14.

Role of nerve growth factor and other trophic factors in brain inflammation.

Villoslada P, Genain CP.

Neuroimmunology Laboratory, Department of Neurology, University of Navarra,
Spain.

Inflammation in the brain is a double-edged process that may be beneficial in
promoting homeostasis and repair, but can also result in tissue injury through
the damaging potential of inflammatory mediators. Thus, control mechanisms that
minimize the extent of the inflammatory reaction are necessary in order to help
preserve brain architecture and restore function.

The expression of neurotrophic factors such as nerve growth factor (NGF) is increased after brain injury, in part mediated by effects on astrocytes of pro-inflammatory mediators and cytokines produced by immune cells. Conversely, cells of the immune system express NGF receptors, and NGF signaling modulates immune function.

Multiple Sclerosis (MS) and the disease model experimental autoimmune encephalomyelitis are neurodegenerative disorders whereby chronic destruction of the brain parenchyma results from an autoaggressive, immune-mediated inflammatory process and insufficient tissue regeneration. Here, we review evidence indicating that the increased production of NGF and other trophic factors in central nervous system (CNS) during these diseases can suppress inflammation by switching the immune response to an anti-inflammatory, suppressive mode in a brain-specific environment.

Thus, trophic factors networks in the adult CNS not only protects
axons and myelin but appear to also actively contribute to the maintenance of
the brain immune privilege. These agents may represent good targets for
therapeutic intervention in MS and other chronic CNS inflammatory diseases.

PMID: 14699976 [PubMed - in process]

[jackD]

1: Iran J Allergy Asthma Immunol. 2006 Dec;5(4):177-81.

Nerve growth factor prevents demyelination, cell death and progression of the disease in experimental allergic encephalomyelitis.

Parvaneh Tafreshi A.
Department of Biochemistry, The national research centre for genetic engineering and biotechnology, Tehran 14155-6343, Iran. tafreshi@nrcgeb.ac.ir

Experimental allergic encephalomyelitis (EAE), a demyelinating disease induced in the animals parallels multiple sclerosis in human in several aspects, provides a useful model to investigate multiple sclerosis.

In this study, we have therefore used this model to study functions of nerve growth factor (NGF) in EAE. NGF with considerable effects on neuron survival, proliferation and differentiation of the nervous system, is also known to act on cells of the immune system. Simultaneous upregulation of proinflammatory cytokines and increased level of NGF points at possible effects of the nerve growth factor in autoimmune diseases. To investigate roles of NGF in experimental allergic encephalomyelitis in vivo, we therefore decided to apply it intracerebroventricularly at a dose of 0.20 mg/mice prior to the induction of EAE.

Our clinical observations showed that in the EAE induced animals who received NGF, severity of the disease was reduced significantly compared to that in saline treated EAE mice. Also neuropathological investigation of spinal cords revealed that in contrast to saline treated EAE mice, no signs of cell death, infiltration and demyelination can be seen in NGF treated EAE mice, suggesting that NGF may have clinical implications in multiple sclerosis.

PMID: 17237570 [PubMed - indexed for MEDLINE]